UV-B-Induced DNA Repair Mechanisms and Their Effects on Mutagenesis and Culturability in Escherichia coli

Abstract

Ultraviolet-B (UV-B) radiation, intensified by ozone depletion, induces DNA damage and promotes mutagenesis, shaping evolution. While UV-induced SOS responses are well characterized in bacteria, the cellular consequences of prolonged UV-B exposure remain less clear. Prolonged UV-B exposure disrupts translation and RecA-mediated SOS induction without major changes in membrane permeability or reactive oxygen species. This impairs mutagenesis and induces a reversible loss of culturability. Genetic analysis reveals both redundant and differential roles for DNA repair pathways: homologous recombination (RecA, RecB), nucleotide excision repair (UvrA), and translesion synthesis (UmuC/D) are essential for maintaining mutagenesis and culturability, while others (RecN, RmuC) have limited impact. Notably, deletion of UvrD (a repair-associated helicase) intensifies transient non-culturability without affecting mutagenesis, underscoring complexity in repair networks. Overall, our findings reveal a dose-dependent trade-off: moderate UV-B promotes mutagenesis with minimal viability loss, whereas prolonged exposure suppresses mutagenesis via transient dormancy, reflecting an adaptive strategy with significant evolutionary implications.